Acid-base disorders have been shown to alter renal handling of calcium. Patients with distal renal tubular acidosis (RTA) often present with hypercalciuria and stones, in contrast, patient with proximal RTA have hypocalciuria. We plan to examine the tubular mechanisms that may be responsible for acid-base induced changes in calcium excretion. In vivo microperfusion technique will be employed in anesthetized rats. Net ion transport rates will be determined from perfusion rates and total calcium concentrations. Electrochemical driving forces across the tubule wall will be calculated from the transepithelial voltages and calcium ion activities. Total calcium and sodium concentrations will be measured by atomic absorption spectrophotometer; bicarbonate concentrations by microcalorimetry, transepithelial voltage, calcium activity pH and PCO2 by conventional and ion selective microelectrodes. In Phase I of the study surface proximal tubules and peritubular capillaries will be perfused with artificial solutions and will examine separate effects of bicarbonate, pH and PCO2 on net calcium transport by this segment of the nephron. In Phase II, we will examine the effects of bicarbonate, pH and PCO2 on calcium transport by the distal tubule. This study will provide important information about the tubular mechanism(s) mediating the abnormal renal calcium handling associated with acid-base disorders and elucidate the fundamental differences in calcium excretion in patients with distal and proximal RTA.